Deep hypothermic circulatory arrest facilitates repair of complex congenital cardiac anomalies in infants. Susceptibility to ischemia of central nervous tissue, however, remains the major limitation to the technique. Investigations in this laboratory have determined that an obstructive lesion of the cerebral microcirculation ("no-reflow phenomenon") which increases in severity with increasing time of normothermic circulatory arrest is abated for up to two hours by deep hypothermia. However, the precise etiology of the no-reflow phenomenon and its casual relationship to cerebral death has not yet been established. Evidence exists that occlusion of capillaries by aggregates (fibrin, rbc, platelet) cannot account for the microcirculatory lesion. This study is designed to systematically determine whether the persistent microcirculatory collapse is related to high intracapillary surface tension relative to local reperfusion pressure (critical opening pressure), or to high extra-vascular pressure (i.e. cellular or interstitial edema). The effect of circulatory arrest and hypothermia on oxidative phosphorylation and lysomes and their relationship to the microcirculatory obstructive lesion will be determined. Mongrel dogs will be subject to circulatory arrest at normothermia, and following combined surface and core cooling with cardiopulmonary bypass. The lysosomal deactivation on the appearance of the no-reflow lesion will be studied.